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Cold agglutinin disease (CAD) is driven by IgM autoantibodies reactive at 80% of patients, but not active on cold-induced peripheral symptoms. Novel drugs include long-acting complement inhibitors, plasma cells, and B-cell targeting agents (proteasome inhibitors, anti-CD38, BTKi, PI3Ki, anti-BAFF). Combination therapy may be the future answer to CAD unmet needs.
Barcellini et al. (Thu,) studied this question.